Neovascularization following traumatic brain injury: possible evidence for both angiogenesis and vasculogenesis

Morgan, Randy; Kreipke, Christian W.; Roberts, George G.; Bagchi, M.; Rafols, José A.

doi:10.1179/016164107x204693

Cited by 66 publications

(59 citation statements)

References 26 publications

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“…Increased capillary density as well as BrdU-positive endothelial cells were observed in both the cortex and hippocampus up to 48 h following experimental TBI (Morgan et al, 2007). It is interesting to note that vessels in and around the contusion site also stained for p-Akt ser, consistent with an active proliferative response.…”

mentioning

confidence: 75%

Temporal and Regional Changes in IGF-1/IGF-1R Signaling in the Mouse Brain after Traumatic Brain Injury

Madathil

Evans

Saatman

2010

Journal of Neurotrauma

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Although neurotrophic factors such as nerve growth factor, basic fibroblast growth factor, brain-derived neurotrophic factor, and neurotrophin 4=5 are elevated after traumatic brain injury (TBI), little is known about the endogenous response of insulin-like growth factor-1 (IGF-1). We evaluated IGF-1, IGF-1 receptor (IGF-1R), and total and phosphorylated Akt (p-Akt), a known downstream mediator of IGF-1 signaling, using ELISA, Western blotting, and immunohistochemistry at 1, 6, 24, 48, and 72 h following 0.5-mm controlled cortical impact brain injury in adult mice. IGF-1 was transiently upregulated in homogenates of injured cortex at 1 h, and cells with increased IGF-1 immunoreactivity were observed in and around the cortical contusion site up to 48 h. IGF-1R and total Akt levels in cortical homogenates were unchanged, although immunohistochemistry revealed regional changes. In contrast, serine p-Akt levels increased significantly in homogenates at 6 h post-injury. Interestingly, delayed increases in vascular IGF-1R, total Akt, and p-Akt immunostaining were observed in and around the cortical contusion. IGF-1 and its downstream mediators were also upregulated in the subcortical white matter. Our findings indicate that moderate TBI results in a brief induction of IGF-1 and its signaling components in the acute post-traumatic period. This may reflect an attempt at endogenous neuroprotection or repair.

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confidence: 75%

Temporal and Regional Changes in IGF-1/IGF-1R Signaling in the Mouse Brain after Traumatic Brain Injury

Madathil

Evans

Saatman

2010

Journal of Neurotrauma

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“…In this study, we have found that this region also harbors cells with angioblast phenotype. Angiogenesis was also observed in other models of traumatic brain injury (Morgan et al 2007), as well as in brain ischemia (Fan and Yang 2007). The formation of novel capillaries is associated with an increased permeability of the walls of pre-existing capillaries and the resultant increase in extravasation of plasma proteins that likely form a scaffold for the new vessels (Dvorak et al 1995).…”

Section: Discussionmentioning

confidence: 92%

Surgical injury-induced early neocortical microvascular changes and characteristics of the cells populating the peri-lesion zone

Sulejczak¹,

Chrapusta²,

Kozłowski³

et al. 2016

Acta Neurobiologiae Experimentalis

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Adult mammalian brain contains a number of specialized neurovascular structures termed "niches" that act as sources of neuronal cells throughout the individual's life. Some of the niches generate neurons to satisfy the need for 'replacement' neurons within the same or closely located brain structures, whereas the other can provide such cells for more distant destinations in the brain. A common characteristic of known neurovascular niches is the presence of a complex 3-dimensional network of basal lamina processes, called fractones. It apparently plays a major role in communication between the various niche-populating cell types as well as in niche activity and output.We hypothesized that similar niches may form ad hoc after a mechanical brain trauma, and tested this possibility in a rat model of surgical brain injury. Four days after removing a small fragment of sensorimotor cortex, the peri-wound region showed numerous symptoms of active repair and remodeling of brain parenchyma, including the presence of multiple cell types of immature phenotypes. The latter, as shown by a variety of light and electron microscopy techniques, included endothelial cell precursors as well as nestin-positive immature neural cells of astrocytic or non-glial characteristics. However, there was no evidence of in situ neurogenesis or a considerable migration of cells from SVZ. The centers of the said repair processes were capillary blood vessels connected with basal lamina-formed fractones. These results indicate that surgical brain trauma causes the formation of a vascular niche with no apparent neurogenic potential.

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“…It has been shown that endothelial cell proliferation and angiogenesis occur after epileptogenic brain injuries, such as TBI and stroke, and angiogenic factors increased following trauma, brain ischemia and inflammation [34][35][36][37][38]. Damage to the BBB and consequent expression of angiogenic factors, proliferation of endothelial cells, and angiogenesis are features common to various epileptogenic insults [25].…”

Section: Discussionmentioning

confidence: 99%

Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy

Zhang

Guo

et al. 2011

Neurochem Res

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Recent studies suggest that angiogenesis and vascular endothelial growth factor (VEGF) are involved in the pathophysiology of epilepsy. However, relatively little data are available linking placenta growth factor (PIGF) with epilepsy. In this study, we assessed concentrations of PIGF in cerebrospinal fluid (CSF) of 60 epileptic patients and 24 non-seizure subjects using sandwich enzyme-linked immunosorbent assays. Epileptic patients in general had higher concentration of CSF-PIGF than controls (7.95 ± 0.88 ng/l vs. 5.87 ± 0.79 ng/l, P < 0.01). CSF-PIGF level in secondary epileptic patients (8.59 ± 1.26 ng/l) was higher than that in idiopathic epileptic patients (7.62 ± 0.20 ng/l) (P < 0.05). In idiopathic epilepsy, CSF-PIGF level in patients with high seizure frequency was higher than those in patients with low seizure frequency and seizure-free in recent 3 years (7.78 ± 0.23 ng/l vs. 7.49 ± 0.09 ng/l and 7.59 ± 0.10 ng/l, P < 0.05). Concentration of CSF-PIGF in patients with a disease duration of > 5 years was higher than those in patients with durations of 1-5 years and <1 year (7.72 ± 0.20 ng/l vs. 7.52 ± 0.09 ng/l and 7.41 ± 0.07 ng/l, P < 0.05). These results indicate that preexisting brain damage, seizure frequency and disease duration are important factors contributing to elevated PIGF.

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Neovascularization following traumatic brain injury: possible evidence for both angiogenesis and vasculogenesis

Abstract: Our results indicated that following TBI, there is a substantial increase in angiogenesis and based on morphologic characterization of BrdU-positive nuclei within the endothelium, we provide evidence for vasculogenesis following injury.

Cited by 66 publications

References 26 publications

Temporal and Regional Changes in IGF-1/IGF-1R Signaling in the Mouse Brain after Traumatic Brain Injury

Temporal and Regional Changes in IGF-1/IGF-1R Signaling in the Mouse Brain after Traumatic Brain Injury

Surgical injury-induced early neocortical microvascular changes and characteristics of the cells populating the peri-lesion zone

Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy

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